Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E2078, a new analgesic is a dynorphin derivative. E2078 shows strong affinity to kappa receptors and is not rapidly cleaved by peptidases. This analgesic is also considered to be free of tolerance and dependence. In the present study, to determine the effect of E2078 on pituitary-adrenocortical function the author administered E2078 (0.001, 0.05, 0.1, 1.0, 10.0 mg.kg-1) by intramuscular injection to 38 adult mongrel dogs under enflurane anesthesia (1.0%) and then investigated the changes in the plasma concentrations of ACTH, cortisol, beta-endorphin, PRA, aldosterone and ADH. In the animal groups which received E2078 at dosages of 0.001, 0.05, 0.1, and 1.0 mg.kg-1, no significant differences in the plasma concentrations of each hormone were detected compared with the control group which received physiological saline by intramuscular injection. However, in the dog group which received E2078 at 10.0 mg.kg-1, the plasma concentrations of PRA and aldosterone were significantly elevated.
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PMID:[Effects of E2078, a new dynorphin derivative, on pituitary-adrenocortical functions in dogs]. 197 31

Opioid peptides are found throughout the central nervous system, and have profound effects on neuroendocrine function. In man, exogenous opiates and opioids elevate circulating prolactin, GH and TSH, and suppress the release of the gonadotrophins and pro-opiocortin-related peptides. However, unlike in other species, there is substantial evidence for a physiological role of endogenous opioids only in the case of the gonadotrophins and ACTH/LPH. Most evidence suggests that LH and FSH are modulated via the hypothalamus or amygdala, where concentrations of opioids and opioid receptors are very high. Endogenous opioids appear to be principally concerned with the frequency-modulated release of GnRH, and this may be important clinically in patients presenting with amenorrhoea. ACTH/LPH are under tonic inhibition by endogenous opioids acting at hypothalamic and/or pituitary levels, and changes in this inhibition may be responsible for the release of these peptides in response to certain forms of stress. It has been reported that the opiate antagonist, naloxone, is clinically useful in paradoxically inhibiting the release of ACTH in patients with Nelson's syndrome, but this requires adequate confirmation. Vasopressin is under biphasic opiate control, but the principal effect is probably opiate-mediated inhibition of vasopressin release. The endogenous ligand for this response is likely to be dynorphin. Suppression of vasopressin release by opiates may become a useful therapy in the treatment of the 'Syndrome of inappropriate ADH'.
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PMID:Brain opiates and neuroendocrine function. 632 67